PEPTIC ULCER

&

UPPER GI BLEEDINGBy

Dr. Abdul QadeerMBBS; FCPS; FICS

Assistant Professor in General Surgery

King Faisal University College of Medicine

Kingdom of Saudi Arabia

OBJECTIVES

1. Definition of peptic ulcer

2. Epidemiology of peptic ulcer

3. Causes of peptic ulcer

4. Clinical presentation

5. Investigations

6. Treatment

7. Definition of upper GI bleeding

8. Epidemiology of upper GI bleeding

9. Causes

10. Clinical presentation

11. Investigations

12. Treatment

1. DEFINITION OF PEPTIC ULCER

A lesion in the lining (mucosa) of the digestive

tract, typically in the stomach or duodenum,

caused by the digestive action of pepsin and

stomach acid.

2. EPIDEMIOLOGY OF PEPTIC ULCER

10% of the population has ulcers

Annual incidence of symptomatic peptic ulcer

is about 0.3%

Duodenal ulcers are 4 times as common as

gastric ulcers and occur at the duodenal cap

Gastric ulcers mostly occur in the lesser

curvature. Usually benign. 5% are malignant

May occur on the stoma following gastric

surgery, esophagus & Meckel’s diverticulum

having ectopic gastric tissue

In general, the ulcer occurs at a junction

between different types of epithelia, the ulcer

occurring in the epithelium least resistant to

acid damage

Gastric malignancy is common in Japan,

Chile, Finland & Iceland due to

environmental & diet factors.

3. CAUSES OF PEPTIC ULCER

Higher pepsin/gastric acid levels, though the

ulcers have been seen in patients having

normal levels

Gastrinoma (Zollinger-Ellison syndrome)

Helicobacter pylori in 80-95% cases

Consumption of NSAIDs

Stress i.e. emotional, trauma, surgical

Injury or death of mucus-producing cells

GASTRINOMA TRIANGLE

CAUSES OF PEPTIC ULCER

Smoking

Alcohol/diet

Hypercalcemia ( calcium secretion)

Genetic factor: first-degree relatives

Blood group O

4. CLINICAL PRESENTATION OF P. ULCER

Pain: epigastric, may radiate to back,

intermittent, may be relieved by eating

Periodicity: the symptoms may disappear

for weeks or months (due to spontaneous

healing)

Vomiting

Alteration in weight:: Weight loss or gain

Bleeding: acute (hematemesis or malena) or

chronic (anemia)

CLINICAL PRESENTATION OF P. ULCER

O/E:

may be normal or epigastric tenderness

Perforation

GOO (Gastric outlet obstruction)

5. INVESTIGATIONS IN PEPTIC ULCER

Gastoduodenoscopy: investigation of

choice, biopsy is taken for histopathology

and tissue for culture, especially H. Pylori

Radiological: Barium meal

Laboratory tests:

a. CLO (Campylobacter-like organism) test

b. Urea breath test (UBT)

c. H.Pylori stool antigen (HpSA) test

CLO TEST KIT

UREA BREATH TEST

6. TREATMENT OF PEPTIC ULCER

Medical treatment:

a) H2-receptor antagonists: cimetidine,

ranitidine, famotidine, nizatidine

b) PPIs: omeprazole, lansoprazole,

esomeprazole, pantoprazole etc.

c) Eradication therapy: PPIs + antibiotics

Surgical treatment:

a) Gastrectomy: Billroth I, Billroth II,

Gastrojejunostomy

b) Vagotomy: Truncal, Selective, Highly

selective

GASTRECTOMY

VAGOTOMY

SEQUELAE OF P.ULCER SURGERY

Recurrent ulceration

Small stomach syndrome

Bile vomiting

Early & late dumping

Post-vagotomy diarrhea

Malignant transformation

Nutritional consequences

Gallstones

DUMPING SYNDROME

EARLY & LATE DUMPING SYNDROMES

7. DEFINITION OF UPPER GI BLEEDING

Where the source of bleeding is in:

Esophagus

Stomach

Duodenum

8. EPIDEMIOLOGY OF UPPER GI BLEEDING

Incidence: 100/100 000 in Western world

Strongly associated with NSAIDs use

5-10% in-hospital mortality

9. CAUSES OF UPPER GI BLEEDING

Ulcers: esophageal, gastric, duodenal

Erosions: esophageal, gastric, duodenal

Mallory-Weiss tear

Esophageal varices

Tumor

Vascular lesions e.g. Dieulafoy’s disease

Aortic-enteric fistula

10. CLINICAL PRESENTATION OF UPPER GI

BLEEDING

Hematemesis

Malena

Associated with GI perforation

Shock

11. INVESTIGATIONS OF UPPER GI BLEEDING

Upper GI endoscopy

Contrast studies

CXR erect posture: diagnostic of GI

perforation

X-RAY CHEST ERECT POSTURE

XRAY ABDOMEN LATERAL DECUBITUS

ENDOSCOPY

BARIUM MEAL

12. TREATMENT OF UPPER GI BLEEDING

Resuscitation

Treat the cause

EMERGENCY MANAGEMENT OF ACUTE NON-VARICEAL

UPPER GIT HAEMORRHAGE

I.V access with large bore cannula

Basic investigations - blood count, routine biochemistry, cross match blood

Hourly measurements of BP, pulse and urine output

I.V colloids or crystalloids –pt with hypotension and tachycardia

Transfuse with blood

Endoscopy for diagnosis & Rx

I.V PPI therapy for bleeding peptic ulcer

EMERGENCY MANAGEMENT OF ACUTE

VARICEAL UPPER GIT BLEEDING

0.9 % saline

Vasopressor(terlipressin)

Prophylactic antibiotics

Emergency endoscope

Variceal band ligation

Proton pump inhibitor

Phosphate enema/lactulose enema

MANAGEMENT OF PEPTIC ULCER

ENDOSCOPIC THERAPY with

* Bipolar electro coagulation

* Heater probe

* Injection therapy

- Absolute alcohol

- 1:10000 epinephrine

* Clips

High dose constant infusion of iv PPI E.g. Omeprazole – 80 mg bolus & 8 mg/hr infusion

PREVENTION OF RECURRENT BLEEDING

Eradication of H.Pylori infection

Discontinue NSAIDS & acids

If NSAIDS have to be used, use along with PPI

Use selective COX-2 inhibitors like Coxib or traditional NSAIDS + Coxib

Coxib + PPI : further significant decrease in ulcers and recurrent bleeding.

MALLORY-WEISS TEARS

Mostly bleeding stops

spontaneously

(Recurrence is only 0-7%)

Endoscopic therapy is only

for actively bleeding

Mallory-Weiss tear.

Angiographic therapy with embolization & operative therapy with over sewing of tear can be done

ESOPHAGEAL VARICES

ESOPHAGEAL VARICES

I. Vasoconstrictors (somatostatin, octreotide, terlipressin) i.v terlipressin infusion at 2 mg 6 hourly, generalized vasoconstriction leading to decreased blood flow to venous system.

II. Baloon tamponade (Sengastaken–Blakemore tube): Triple lumen or Four lumen tube with esophageal and gastric balloons.

III. Endoscopic variceal ligation (Band ligation)

IV. Sclerotherapy

V. Antibiotic therapy

SENGASTAKEN-BLAKEMORE TUBE

Quinolones – for patients with cirrhosis

decreases the bacterial infection & mortality.

Non selective Beta blockers – Propranolol,

Nadolol

For recurrent esophageal bleeding –

continue therapy with beta blocker +

endoscopic ligation

If not subsided with medical therapy, Go for

INVASIVE THERAPY:

TIPSS (Transjugular intrahepatic

portosystemic shunt)

Other shunts e.g. Danver

GASTRITIS

Avoiding the long-term use

of alcohol, NSAIDs, coffee,

high-fat foods and drugs

Reducing stress through

relaxation techniques

Antacids, H2 blockers, PPIs

Triple therapy: 2 antibiotics + a PPI is commonly used to treat H. Pylori related gastritis

THE END